WildLife Group
of the SAVA
Botulism in Wild Birds
Dr R D Last – BVSc; M.Med.Vet (Pathology)
Avian botulism is a neurological disease of birds
characterized by flaccid paralysis of voluntary
muscles, due to the ingestion of preformed botulinum
neurotoxin produced by the bacterium Clostridium
botulinum. This condition is considered as the most
common cause of die offs in wild bird populations
worldwide. waterfowl, shorebirds, fish eating birds, birds that
feed on maggots and avians which frequent landfill
sites are considered at highest risk of developing
botulism. Botulism in wild raptors is usually associated
with improper disposal of poultry carcasses. Vultures
appear to be resistant to the botulism toxin.
Clostridium botulinum is a soil living bacterium that
can produce environmentally resistance spores.
These spores are highly resistant to desiccation
and extreme temperatures, and themselves are
harmless, until the correct environmental factors and
anaerobic conditions stimulate them to germinate and
undergo vegetative growth. Under certain conditions
(increased temperature, high levels of organic
material in sediment, low water levels, high water pH,
low water oxygen content / anaerobic conditions and
increased water salinity) spores germinate and grow
producing large quantities of toxin. Raw sewage and
rotting vegetation are also suitable substrates for toxin
production. This bacterium is particularly common
in wetland environments, but also grows well in
decomposing carcasses. Toxins can also accumulate
in fish as well as invertebrate hosts such as aquatic
insects, molluscs and crustacea, as well as maggots
feeding on decomposed carcasses. Disease transmission is thought to occur through a
variety of mechanisms including
There are seven distinct types of neurotoxins
produced by Clostridium botulinum (A-G), with most
isolates producing only one type of neurotoxin,
although isolates that produce multiple toxins do
occur. Avian botulism is well described in wild
birds being most frequently reported in waterfowl
(ducks, geese, swans), Ibis, egrets and pelicans. Most
wild avian mortalities, particularly in waterfowl,
are associated with type C toxin or the type C/D
mosaic, while type E toxin has been associated with
mortalities among fish eating birds. Filter feeding
12
• Carcass-maggot cycle where dead fish and birds
washing up on beaches of ocean wetlands, lakes
and ponds can become sources for C. botulinum
growth. Shorebirds and maggot eating birds may
then ingest the toxins as they feed on maggots
and carrion beetles in these decomposing
carcasses. Thousands of toxic maggots can be
produced from a single carcass. Ingestion of
just two to four toxic maggots can kill a bird and
further perpetuate the cycle.
• Some mussel populations are believed to
create favorable habitat for C. botulinum and
accumulate the toxin with no ill effects. These
mussels then facilitate the transport of the toxin
up the food chain as they are consumed by fish
which are in turn consumed by fish-eating water
birds.
• Prolific growth of algae (blooms) is also believed
to contribute to avian botulism outbreaks
through the creation of decaying mats of
sloughed algae which may lead to low water
oxygen levels and a rich growth nutrient medium.
This creates an ideal environment for the
vegetative state of C. botulinum and resultant
toxin production.